The Amazing World of Psychiatry: A Psychiatry Bloghttps://theamazingworldofpsychiatry.wordpress.com
by Dr Justin MarleyThu, 17 Aug 2017 20:56:36 +0000enhourly1http://wordpress.com/https://s2.wp.com/i/buttonw-com.pngThe Amazing World of Psychiatry: A Psychiatry Bloghttps://theamazingworldofpsychiatry.wordpress.com
The Brain Hypometabolism Hypothesis Part 110: (Harreveld, 1959)https://theamazingworldofpsychiatry.wordpress.com/2017/08/17/the-brain-hypometabolism-hypothesis-part-110-harreveld-1959/
https://theamazingworldofpsychiatry.wordpress.com/2017/08/17/the-brain-hypometabolism-hypothesis-part-110-harreveld-1959/#respondThu, 17 Aug 2017 20:55:28 +0000http://theamazingworldofpsychiatry.wordpress.com/?p=18337]]>Lai, Zhang and Wang have written about the NMDA receptor and excitotoxicity in their paper.

The authors cite an important study by Harreveld which identifies a role for Glutamate and led to the suggestion that Glutamate mediates stroke related brain injury (Harreveled, 1959). This study provided evidence that an extract from the Pallium induced Cortical depression and muscle contraction.

Context

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

The NMDA Receptor is an ion channel which is activated by Glutamate. The NMDA Receptor is involved in the response of neurons to ischaemia. The NMDA Receptor is also involved in memory formation in a process referred to as Long Term Potentiation.

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

Lai, Zhang and Wang outline the role of Monosodium Glutamate in their paper. Monosodium Glutamate is a food additive. In a paper published in 1957, Lucas and Newhhouse reported the results of their study looking at the effects of Monosodium Glutamate (MSG) when applied to the mouse retina. The researchers found evidence of neurotoxicity. Further findings confirmed that Glutamate (MSG dissociates into Sodium and Glutamate in solution) is excitatory (i.e. increases the chance of a neuron firing).

What is Excitotoxicity?

Excitoxicity is the damage and death of neurons secondary to Glutamate receptor activation. There is an interesting paper by Lai, Zhang and Wang on excitotoxicity and stroke. The authors look at the targets for neuroprotection following a stroke. Excitotoxicity is related to the NMDA Receptor. This in turn is relevant to the Brain Hypometabolism Hypothesis.

In their paper Lai, Zhang and Wang write that although excitotoxicity was initially investigated in relation to the properties of Monosodium Glutamate it plays an important role in brain trauma and a number of neurodegenerative conditions including

Huntington’s Disease

Alzheimer’s Disease

Amyotrophic Lateral Sclerosis

Excitotoxicity and Excitation

Professor John Olney and colleagues conducted research in 1971 into the excitotoxic effects of Glutamate analogues (Olney et al, 1971). They found that analogues which were excitatory were excitotoxic and those which were not excitatory were not excitotoxic. Contextualising this – the effects of Glutamate are mediated via the NMDA Receptor and excitotoxicity is a pathological process which can result from reduced energy metabolism. This in turn is relevant to the Brain Hypometabolism Hypothesis.

Summarising this:

Excitatory properties are required for excitoxicity

Brain Hypometabolism Hypothesis

The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that

There are several key pathways in energy metabolism in humans. Several pathways result in the formation of Acetyl CoA from fatty acids, amino acids and glucose. Acetyl CoA is utilised in the Citric Acid Cycle. The Citric Acid Cycle generates ATP. The Citric Acid Cycle also generates NADH which is used in Oxidative Phosphorylation which utilises Oxygen as an electron acceptor.

What is Glycolysis?

Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.

The Citric Acid Cycle is one of the main energy metabolism pathways in humans. Acetyl Co-A which is generated from other pathways is utilised in the Citric Acid Cycle. The Citric Acid Cycle has a number of properties

Generation of energy in the form of ATP

Generating NADH which is utilised in oxidative phosphorylation

Citric Acid is regenerated

Carbon Dioxide is produced

The Citric Acid Cycle takes place in the Mitochondria.

What is Oxidative Phosphorylation?

Oxidative phosphorylation is a series of chemical reactions in which electrons are transferred, nutrients are metabolised and ATP is formed. Nutrients are oxidised and the donated electrons are processed in the electron transport chain. ATP formation via ATP Synthase utilises the electron/proton gradient across the mitochondrial membrane according to the Chemiosmotic Theory.

What is the Chemiosmotic Theory?

The Chemiosmotic Theory is central to the understanding of Oxidative Phosphorylation. Proposed by Dr Peter Mitchell in 1961, the theory states that the energy for ATP generation derives from electrical and chemical gradients resulting from the transfer of electrons and protons across the mitochondrial membrane in the electron transport chain.

The first step in Oxidative Phosphorylation in humans is the transfer of electrons from NAD via Complex I. The structure of Complex I is shown above. Complex I is also known as NADH-coenzyme Q Oxidoreductase. NADH donates electrons to Complex I in a reaction requiring Coenzyme Q10. The electrons are further transferred via Flavin Mononucleotide and Iron-Sulfur Complexes before the transfer of proteins into the intermembrane space.

Complex II is involved in Oxidative Phosphorylation and is also known as Succinate Dehydrogenase. Succinate is oxidised (donating electrons) to form Fumarate. The donated electrons enter the electron transport chain.

Complex III is also known as Q-cytochrome C Oxidoreductase. Complex III contains Cytochromes. Ubiquinol (a reduced form of Coenzyme Q10) donates electrons to Cytochrome C. Electrons are transferred between molecules in a circuit which causes four protons to be transferred across the Mitochondrial membrane for every 2 electrons. This forms part of the electron transport chain.

ATP Synthase is an enzyme that combines inorganic phosphate and Adenosine Diphosphate to form Adenosine Triphosphate (ATP). This in turn is used as a source of energy.

Complex IV is also known as Cytochrome C Oxidase. Complex IV contains Heme groups, Copper, Magnesium and Zinc. Complex IV facilitates the transfer of electrons to Oxygen in a reaction which results in the formation of water.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

Kierkegaard and colleagues have published an interesting paper in which they investigate Health Information Exchange usage with a qualitative study. They identify the following 8 themes in Table 4.

Purpose of Usage

Frequency of Usage

Availability of Information

Patient Consent

Healthcare Organisation Participation

Non-RHIO Related Exchange Mechanisms

Search Confidence

Usability

Context

Patient Records

Patient records are central to the delivery of healthcare and serve a number of functions including the recording of clinical assessments and interventions. Aggregated data is also utilised at a local and national level to inform commissioning.

Electronic Patient Records

The digitisation of patient records offers a number of advantages over paper based records. These advantages include automated backup of records, reduced use of physical storage space (since paper based notes are switched to servers), off-site access to records using mobile devices and the potential to develop analytical clinical support tools which use computers to process clinical data to help improve clinical decisions. Not all healthcare services have electronic patient records but most providers are moving in this direction.

Getting Electronic Patient Records to Talk to Each Other

When patients move between healthcare providers – for instance between primary care and the hospital – they may find that one provider does not have information that the other provider has. There are many providers and many electronic paper record systems. For two systems to talk to each other they have to solve a number of problems. When these problems are solved a patient can move between providers and healthcare information can be accessed by the different providers. A key solution to this problem of health information gaps is the Health Information Exchange (HIE).

The Health Information Exchange

There are many definitions of what a Health Information Exchange is. (Hersh et al, 2015) define a HIE as follows:

Whilst this definition is simple, the process of sharing clinical information between healthcare organisations is technically complex and encompasses a range of software, hardware and governance issues. The process of helping systems to talk to each other is helped by the development of standards. A set of standards is outlined in the NHS interoperability framework.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

]]>https://theamazingworldofpsychiatry.wordpress.com/2017/08/16/health-information-exchange-themes-from-kierkegaard-et-al-2014/feed/0Dr Justin Marleycomputer-keyboard-1380475577zzmThe Brain Hypometabolism Hypothesis Part 109: The C-Terminus of NMDA Receptor Subunitshttps://theamazingworldofpsychiatry.wordpress.com/2017/08/15/the-brain-hypometabolism-hypothesis-part-109-the-c-terminus-of-nmda-receptor-subunits/
https://theamazingworldofpsychiatry.wordpress.com/2017/08/15/the-brain-hypometabolism-hypothesis-part-109-the-c-terminus-of-nmda-receptor-subunits/#respondTue, 15 Aug 2017 07:14:42 +0000http://theamazingworldofpsychiatry.wordpress.com/?p=18314]]>Lai, Zhang and Wang have written about the NMDA receptor and excitotoxicity in their paper.

They note that the C-Terminus of the NMDA receptor subunits Glu2NA and Glu2NB mediates function and swapping the C-Terminus between the subunits changes the functional properties.

Context

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

Lai, Zhang and Wang outline the role of Monosodium Glutamate in their paper. Monosodium Glutamate is a food additive. In a paper published in 1957, Lucas and Newhhouse reported the results of their study looking at the effects of Monosodium Glutamate (MSG) when applied to the mouse retina. The researchers found evidence of neurotoxicity. Further findings confirmed that Glutamate (MSG dissociates into Sodium and Glutamate in solution) is excitatory (i.e. increases the chance of a neuron firing).

What is Excitotoxicity?

Excitoxicity is the damage and death of neurons secondary to Glutamate receptor activation. In their paper Lai, Zhang and Wang write about excitotoxicity and stroke. The authors look at the targets for neuroprotection following a stroke. Excitotoxicity is related to the NMDA Receptor. This in turn is relevant to the Brain Hypometabolism Hypothesis.

In their paper Lai, Zhang and Wang write that although excitotoxicity was initially investigated in relation to the properties of Monosodium Glutamate it plays an important role in brain trauma and a number of neurodegenerative conditions including

Huntington’s Disease

Alzheimer’s Disease

Amyotrophic Lateral Sclerosis

Excitotoxicity and Excitation

Professor John Olney and colleagues conducted research in 1971 into the excitotoxic effects of Glutamate analogues (Olney et al, 1971). They found that analogues which were excitatory were excitotoxic and those which were not excitatory were not excitotoxic. Contextualising this – the effects of Glutamate are mediated via the NMDA Receptor and excitotoxicity is a pathological process which can result from reduced energy metabolism. This in turn is relevant to the Brain Hypometabolism Hypothesis.

Summarising this:

Excitatory properties are required for excitoxicity

Brain Hypometabolism Hypothesis

The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that

‘Energy hypometabolism in the brain leads to neuropathology‘

Key Pathways in Energy Metabolism

There are several key pathways in energy metabolism in humans. Several pathways result in the formation of Acetyl CoA from fatty acids, amino acids and glucose. Acetyl CoA is utilised in the Citric Acid Cycle. The Citric Acid Cycle generates ATP. The Citric Acid Cycle also generates NADH which is used in Oxidative Phosphorylation which utilises Oxygen as an electron acceptor.

What is Glycolysis?

Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.

The Citric Acid Cycle is one of the main energy metabolism pathways in humans. Acetyl Co-A which is generated from other pathways is utilised in the Citric Acid Cycle. The Citric Acid Cycle has a number of properties

Generation of energy in the form of ATP

Generating NADH which is utilised in oxidative phosphorylation

Citric Acid is regenerated

Carbon Dioxide is produced

The Citric Acid Cycle takes place in the Mitochondria.

What is Oxidative Phosphorylation?

Oxidative phosphorylation is a series of chemical reactions in which electrons are transferred, nutrients are metabolised and ATP is formed. Nutrients are oxidised and the donated electrons are processed in the electron transport chain. ATP formation via ATP Synthase utilises the electron/proton gradient across the mitochondrial membrane according to the Chemiosmotic Theory.

What is the Chemiosmotic Theory?

The Chemiosmotic Theory is central to the understanding of Oxidative Phosphorylation. Proposed by Dr Peter Mitchell in 1961, the theory states that the energy for ATP generation derives from electrical and chemical gradients resulting from the transfer of electrons and protons across the mitochondrial membrane in the electron transport chain.

The first step in Oxidative Phosphorylation in humans is the transfer of electrons from NAD via Complex I. The structure of Complex I is shown above. Complex I is also known as NADH-coenzyme Q Oxidoreductase. NADH donates electrons to Complex I in a reaction requiring Coenzyme Q10. The electrons are further transferred via Flavin Mononucleotide and Iron-Sulfur Complexes before the transfer of proteins into the intermembrane space.

Complex II is involved in Oxidative Phosphorylation and is also known as Succinate Dehydrogenase. Succinate is oxidised (donating electrons) to form Fumarate. The donated electrons enter the electron transport chain.

Complex III is also known as Q-cytochrome C Oxidoreductase. Complex III contains Cytochromes. Ubiquinol (a reduced form of Coenzyme Q10) donates electrons to Cytochrome C. Electrons are transferred between molecules in a circuit which causes four protons to be transferred across the Mitochondrial membrane for every 2 electrons. This forms part of the electron transport chain.

ATP Synthase is an enzyme that combines inorganic phosphate and Adenosine Diphosphate to form Adenosine Triphosphate (ATP). This in turn is used as a source of energy.

Complex IV is also known as Cytochrome C Oxidase. Complex IV contains Heme groups, Copper, Magnesium and Zinc. Complex IV facilitates the transfer of electrons to Oxygen in a reaction which results in the formation of water.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

Kierkegaard and colleagues have published an interesting paper in which they investigate Health Information Exchange usage with a qualitative study. This contrasts with the (Vest et al, 2014) paper which is a quantitative study.

Context

Patient Records

Patient records are central to the delivery of healthcare and serve a number of functions including the recording of clinical assessments and interventions. Aggregated data is also utilised at a local and national level to inform commissioning.

Electronic Patient Records

The digitisation of patient records offers a number of advantages over paper based records. These advantages include automated backup of records, reduced use of physical storage space (since paper based notes are switched to servers), off-site access to records using mobile devices and the potential to develop analytical clinical support tools which use computers to process clinical data to help improve clinical decisions. Not all healthcare services have electronic patient records but most providers are moving in this direction.

Getting Electronic Patient Records to Talk to Each Other

When patients move between healthcare providers – for instance between primary care and the hospital – they may find that one provider does not have information that the other provider has. There are many providers and many electronic paper record systems. For two systems to talk to each other they have to solve a number of problems. When these problems are solved a patient can move between providers and healthcare information can be accessed by the different providers. A key solution to this problem of health information gaps is the Health Information Exchange (HIE).

The Health Information Exchange

There are many definitions of what a Health Information Exchange is. (Hersh et al, 2015) define a HIE as follows:

Whilst this definition is simple, the process of sharing clinical information between healthcare organisations is technically complex and encompasses a range of software, hardware and governance issues. The process of helping systems to talk to each other is helped by the development of standards. A set of standards is outlined in the NHS interoperability framework.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

They cite evidence to suggest that NMDA Receptor GLU2NBR antagonists are neuroprotective and the opposite may be the case for GLU2NAR antagonists.

Context

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

Lai, Zhang and Wang outline the role of Monosodium Glutamate in their paper. Monosodium Glutamate is a food additive. In a paper published in 1957, Lucas and Newhhouse reported the results of their study looking at the effects of Monosodium Glutamate (MSG) when applied to the mouse retina. The researchers found evidence of neurotoxicity. Further findings confirmed that Glutamate (MSG dissociates into Sodium and Glutamate in solution) is excitatory (i.e. increases the chance of a neuron firing).

What is Excitotoxicity?

Excitoxicity is the damage and death of neurons secondary to Glutamate receptor activation. There is an interesting paper by Lai, Zhang and Wang on excitotoxicity and stroke. The authors look at the targets for neuroprotection following a stroke. Excitotoxicity is related to the NMDA Receptor. This in turn is relevant to the Brain Hypometabolism Hypothesis.

In their paper Lai, Zhang and Wang write that although excitotoxicity was initially investigated in relation to the properties of Monosodium Glutamate it plays an important role in brain trauma and a number of neurodegenerative conditions including

Huntington’s Disease

Alzheimer’s Disease

Amyotrophic Lateral Sclerosis

Excitotoxicity and Excitation

Professor John Olney and colleagues conducted research in 1971 into the excitotoxic effects of Glutamate analogues (Olney et al, 1971). They found that analogues which were excitatory were excitotoxic and those which were not excitatory were not excitotoxic. Contextualising this – the effects of Glutamate are mediated via the NMDA Receptor and excitotoxicity is a pathological process which can result from reduced energy metabolism. This in turn is relevant to the Brain Hypometabolism Hypothesis.

Summarising this:

Excitatory properties are required for excitoxicity

Brain Hypometabolism Hypothesis

The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that

‘Energy hypometabolism in the brain leads to neuropathology‘

Key Pathways in Energy Metabolism

There are several key pathways in energy metabolism in humans. Several pathways result in the formation of Acetyl CoA from fatty acids, amino acids and glucose. Acetyl CoA is utilised in the Citric Acid Cycle. The Citric Acid Cycle generates ATP. The Citric Acid Cycle also generates NADH which is used in Oxidative Phosphorylation which utilises Oxygen as an electron acceptor.

What is Glycolysis?

Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.

The Citric Acid Cycle is one of the main energy metabolism pathways in humans. Acetyl Co-A which is generated from other pathways is utilised in the Citric Acid Cycle. The Citric Acid Cycle has a number of properties

Generation of energy in the form of ATP

Generating NADH which is utilised in oxidative phosphorylation

Citric Acid is regenerated

Carbon Dioxide is produced

The Citric Acid Cycle takes place in the Mitochondria.

What is Oxidative Phosphorylation?

Oxidative phosphorylation is a series of chemical reactions in which electrons are transferred, nutrients are metabolised and ATP is formed. Nutrients are oxidised and the donated electrons are processed in the electron transport chain. ATP formation via ATP Synthase utilises the electron/proton gradient across the mitochondrial membrane according to the Chemiosmotic Theory.

What is the Chemiosmotic Theory?

The Chemiosmotic Theory is central to the understanding of Oxidative Phosphorylation. Proposed by Dr Peter Mitchell in 1961, the theory states that the energy for ATP generation derives from electrical and chemical gradients resulting from the transfer of electrons and protons across the mitochondrial membrane in the electron transport chain.

The first step in Oxidative Phosphorylation in humans is the transfer of electrons from NAD via Complex I. The structure of Complex I is shown above. Complex I is also known as NADH-coenzyme Q Oxidoreductase. NADH donates electrons to Complex I in a reaction requiring Coenzyme Q10. The electrons are further transferred via Flavin Mononucleotide and Iron-Sulfur Complexes before the transfer of proteins into the intermembrane space.

Complex II is involved in Oxidative Phosphorylation and is also known as Succinate Dehydrogenase. Succinate is oxidised (donating electrons) to form Fumarate. The donated electrons enter the electron transport chain.

Complex III is also known as Q-cytochrome C Oxidoreductase. Complex III contains Cytochromes. Ubiquinol (a reduced form of Coenzyme Q10) donates electrons to Cytochrome C. Electrons are transferred between molecules in a circuit which causes four protons to be transferred across the Mitochondrial membrane for every 2 electrons. This forms part of the electron transport chain.

ATP Synthase is an enzyme that combines inorganic phosphate and Adenosine Diphosphate to form Adenosine Triphosphate (ATP). This in turn is used as a source of energy.

Complex IV is also known as Cytochrome C Oxidase. Complex IV contains Heme groups, Copper, Magnesium and Zinc. Complex IV facilitates the transfer of electrons to Oxygen in a reaction which results in the formation of water.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

There is an interesting paper by Vest and colleagues titled ‘Association Between Use of a Health Information Exchange System and Hospital Admissions’.

This is an American study which looks at the use of a Health Information Exchange (HIE) in New York State. The researchers looked at a sample of 15,645 patients seen in the Emergency Department.

Here are a few reflections:

Several Odds Ratios are identified in the paper.

Since there are multiple comparisons there would be benefit from a correction (e.g. Bonferroni correction).

A null hypothesis would help to discriminate between the primary and secondary analysis.

A power calculation would identify the numbers required for the analysis

The same-day HIE access analysis is impacted by reduced numbers in this sample set for which point 4 is relevant.

What was also interesting was that the retrospective collection of data although providing utility impacted on the questions. A key issue thrown up by the analysis is the approach to accessing the HIE in relation to decision making.

What Does the Odds Ratio Mean?

The odds ratios tells us about a relationship between two things. In the clinical setting these two things might be expected to have a causal relationship e.g. Blood Pressure and exercise.

How is it Calculated?

Taking the Blood Pressure example. Let’s suppose that a group of people have their Blood Pressure checked before and after an exercise/non-exercise intervention. Let’s also suppose that people are classed as doing regular exercise (intervention) or not doing regular exercise (non-exercise).

We want to see if there is a relationship between the two and it would be great if we could have a number to sum up that relationship. Let’s also suppose that we think the relationship is ‘Doing regular exercise reduces Blood Pressure’. The exposure is doing regular exercise and the outcome is reduced Blood Pressure.

Let’s suppose there are 100 people in the study (These are illustrative numbers only). 60 people do regular exercise and 50 people have low Blood Pressure. Of the 60 people that do regular exercise 40 people have low Blood Pressure. I will write this out in the following statements

60 people do regular exercise and 40 have reduced Blood Pressure

60 people do regular exercise and 20 have high Blood Pressure

40 people do not do regular exercise and 10 have reduced Blood Pressure

40 people do not do regular exercise and 30 have high Blood Pressure

Before we can talk about the odds ratio we need to look at probabilities and also clarify which relationship we are examining.

Firstly let us look at some probabilities.

What is the probability that someone who is in the exercise intervention group will have reduced Blood Pressure?

This would be 40/60 or 0.67 (2 significant figures). Just to explain – if someone is in the exercise group then we know that 40 have reduced Blood Pressure and 20 have high Blood Pressure. The probability is the ratio of the outcome of interest to all of the outcomes in that group. Therefore this is 40/60.

What is the probability that someone who is in the exercise intervention group will have high Blood Pressure?

The reasoning is much the same as the example above except we are substituting 20 for 40 i.e. the probability is 20/60 or 0.33 (2 significant figures).

What is the probability that someone who is in the non-exercise group will have lower Blood Pressure?

This will be 10/40 or 0.25

What is the probability that someone who is in the non-exercise group will have high Blood Pressure?

This will be 30/40 or 0.75

Now we can turn to the odds ratio which is the ratio of probabilities.

What is the odds of having high Blood Pressure with exercise compared to non-exercise.

The probability of high Blood Pressure given exercise is 0.33.

The probability of high Blood Pressure given non-exercise is 0.75

The odds ratio of having high Blood Pressure with exercise compared to non-exercise is 0.33/0.75 = 0.44

We can have several odds ratios in the same sample – it depends on what question we are asking.

What is the odds of having lower Blood Pressure with exercise compared to non-exercise.

The probability of lower Blood Pressure given exercise is 0.67

The probability of lower Blood Pressure given exercise is 0.25

The odds ratio of having lower Blood Pressure with exercise compared to non-exercise is 0.67/0.25 = 2.68.

So just to summarise the odds ratio is a ratio of probabilities. You need to work out the probabilities first. Then you need to clearly state the relationship you are interested in and then calculate the ratio of the probabilities for that relationship.

Finally just a few key points.

The odds ratio can be between 0 and infinity. So for example if all the people in the non-exercise intervention group had high Blood Pressure then the odds ratio of having lower Blood Pressure with exercise compared to non-exercise would be infinity (assuming all other figures remained the same).
The odds ratio can be affected by sample bias. So if the sample is not characteristic of the general population and is small then the odds ratio could be abnormally high or low. The confidence interval is usually calculated for the odds ratio although this can be a little complicated.

Other Links

There is a good explanation of the odds ratio in this paper.

Context

Patient Records

Patient records are central to the delivery of healthcare and serve a number of functions including the recording of clinical assessments and interventions. Aggregated data is also utilised at a local and national level to inform commissioning.

Electronic Patient Records

The digitisation of patient records offers a number of advantages over paper based records. These advantages include automated backup of records, reduced use of physical storage space (since paper based notes are switched to servers), off-site access to records using mobile devices and the potential to develop analytical clinical support tools which use computers to process clinical data to help improve clinical decisions. Not all healthcare services have electronic patient records but most providers are moving in this direction.

Getting Electronic Patient Records to Talk to Each Other

When patients move between healthcare providers – for instance between primary care and the hospital – they may find that one provider does not have information that the other provider has. There are many providers and many electronic paper record systems. For two systems to talk to each other they have to solve a number of problems. When these problems are solved a patient can move between providers and healthcare information can be accessed by the different providers. A key solution to this problem of health information gaps is the Health Information Exchange (HIE).

The Health Information Exchange

There are many definitions of what a Health Information Exchange is. (Hersh et al, 2015) define a HIE as follows:

Whilst this definition is simple, the process of sharing clinical information between healthcare organisations is technically complex and encompasses a range of software, hardware and governance issues. The process of helping systems to talk to each other is helped by the development of standards. A set of standards is outlined in the NHS interoperability framework.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

]]>https://theamazingworldofpsychiatry.wordpress.com/2017/08/07/reflections-on-health-information-exchange-use-in-vest-et-al-2014/feed/0Dr Justin Marleycomputer-keyboard-1380475577zzmThe Brain Hypometabolism Hypothesis Part 107: GLU2NA, GLU2NB and Synaptic Plasticityhttps://theamazingworldofpsychiatry.wordpress.com/2017/08/06/the-brain-hypometabolism-hypothesis-part-107-glu2na-glu2nb-and-synaptic-plasticity/
https://theamazingworldofpsychiatry.wordpress.com/2017/08/06/the-brain-hypometabolism-hypothesis-part-107-glu2na-glu2nb-and-synaptic-plasticity/#respondSun, 06 Aug 2017 07:54:27 +0000http://theamazingworldofpsychiatry.wordpress.com/?p=18253]]>Lai, Zhang and Wang have written about the NMDA receptor and excitotoxicity in their paper.

They note that two NMDA Receptor subunits – GLU2NA and GLU2NB interact with proteins involved in synaptic plasticity – in Long Term Depression (LTD) and Long Term Potentiation (LTP).

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

Lai, Zhang and Wang outline the role of Monosodium Glutamate in their paper. Monosodium Glutamate is a food additive. In a paper published in 1957, Lucas and Newhhouse reported the results of their study looking at the effects of Monosodium Glutamate (MSG) when applied to the mouse retina. The researchers found evidence of neurotoxicity. Further findings confirmed that Glutamate (MSG dissociates into Sodium and Glutamate in solution) is excitatory (i.e. increases the chance of a neuron firing).

What is Excitotoxicity?

Excitoxicity is the damage and death of neurons secondary to Glutamate receptor activation. There is an interesting paper by Lai, Zhang and Wang on excitotoxicity and stroke. The authors look at the targets for neuroprotection following a stroke. Excitotoxicity is related to the NMDA Receptor. This in turn is relevant to the Brain Hypometabolism Hypothesis.

In their paper Lai, Zhang and Wang write that although excitotoxicity was initially investigated in relation to the properties of Monosodium Glutamate it plays an important role in brain trauma and a number of neurodegenerative conditions including

Huntington’s Disease

Alzheimer’s Disease

Amyotrophic Lateral Sclerosis

Excitotoxicity and Excitation

Professor John Olney and colleagues conducted research in 1971 into the excitotoxic effects of Glutamate analogues (Olney et al, 1971). They found that analogues which were excitatory were excitotoxic and those which were not excitatory were not excitotoxic. Contextualising this – the effects of Glutamate are mediated via the NMDA Receptor and excitotoxicity is a pathological process which can result from reduced energy metabolism. This in turn is relevant to the Brain Hypometabolism Hypothesis.

Summarising this:

Excitatory properties are required for excitoxicity

Brain Hypometabolism Hypothesis

The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that

‘Energy hypometabolism in the brain leads to neuropathology‘

Key Pathways in Energy Metabolism

There are several key pathways in energy metabolism in humans. Several pathways result in the formation of Acetyl CoA from fatty acids, amino acids and glucose. Acetyl CoA is utilised in the Citric Acid Cycle. The Citric Acid Cycle generates ATP. The Citric Acid Cycle also generates NADH which is used in Oxidative Phosphorylation which utilises Oxygen as an electron acceptor.

What is Glycolysis?

Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.

The Citric Acid Cycle is one of the main energy metabolism pathways in humans. Acetyl Co-A which is generated from other pathways is utilised in the Citric Acid Cycle. The Citric Acid Cycle has a number of properties

Generation of energy in the form of ATP

Generating NADH which is utilised in oxidative phosphorylation

Citric Acid is regenerated

Carbon Dioxide is produced

The Citric Acid Cycle takes place in the Mitochondria.

What is Oxidative Phosphorylation?

Oxidative phosphorylation is a series of chemical reactions in which electrons are transferred, nutrients are metabolised and ATP is formed. Nutrients are oxidised and the donated electrons are processed in the electron transport chain. ATP formation via ATP Synthase utilises the electron/proton gradient across the mitochondrial membrane according to the Chemiosmotic Theory.

What is the Chemiosmotic Theory?

The Chemiosmotic Theory is central to the understanding of Oxidative Phosphorylation. Proposed by Dr Peter Mitchell in 1961, the theory states that the energy for ATP generation derives from electrical and chemical gradients resulting from the transfer of electrons and protons across the mitochondrial membrane in the electron transport chain.

The first step in Oxidative Phosphorylation in humans is the transfer of electrons from NAD via Complex I. The structure of Complex I is shown above. Complex I is also known as NADH-coenzyme Q Oxidoreductase. NADH donates electrons to Complex I in a reaction requiring Coenzyme Q10. The electrons are further transferred via Flavin Mononucleotide and Iron-Sulfur Complexes before the transfer of proteins into the intermembrane space.

Complex II is involved in Oxidative Phosphorylation and is also known as Succinate Dehydrogenase. Succinate is oxidised (donating electrons) to form Fumarate. The donated electrons enter the electron transport chain.

Complex III is also known as Q-cytochrome C Oxidoreductase. Complex III contains Cytochromes. Ubiquinol (a reduced form of Coenzyme Q10) donates electrons to Cytochrome C. Electrons are transferred between molecules in a circuit which causes four protons to be transferred across the Mitochondrial membrane for every 2 electrons. This forms part of the electron transport chain.

ATP Synthase is an enzyme that combines inorganic phosphate and Adenosine Diphosphate to form Adenosine Triphosphate (ATP). This in turn is used as a source of energy.

Complex IV is also known as Cytochrome C Oxidase. Complex IV contains Heme groups, Copper, Magnesium and Zinc. Complex IV facilitates the transfer of electrons to Oxygen in a reaction which results in the formation of water.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

There is an interesting paper by Vest and colleagues titled ‘Association Between Use of a Health Information Exchange System and Hospital Admissions’.

This is an American study which looks at the use of a Health Information Exchange (HIE) in New York State. The researchers looked at a sample of 15,645 patients seen in the Emergency Department.

The main finding was that in their sample the Odds Ratio for an admission when a HIE was accessed compared to when it was not accessed was 0.70. In other words there was a 30% reduction in admissions if a HIE was used.

What Does the Odds Ratio Mean?

The odds ratios tells us about a relationship between two things. In the clinical setting these two things might be expected to have a causal relationship e.g. Blood Pressure and exercise.

How is it Calculated?

Taking the Blood Pressure example. Let’s suppose that a group of people have their Blood Pressure checked before and after an exercise/non-exercise intervention. Let’s also suppose that people are classed as doing regular exercise (intervention) or not doing regular exercise (non-exercise).

We want to see if there is a relationship between the two and it would be great if we could have a number to sum up that relationship. Let’s also suppose that we think the relationship is ‘Doing regular exercise reduces Blood Pressure’. The exposure is doing regular exercise and the outcome is reduced Blood Pressure.

Let’s suppose there are 100 people in the study (These are illustrative numbers only). 60 people do regular exercise and 50 people have low Blood Pressure. Of the 60 people that do regular exercise 40 people have low Blood Pressure. I will write this out in the following statements

60 people do regular exercise and 40 have reduced Blood Pressure

60 people do regular exercise and 20 have high Blood Pressure

40 people do not do regular exercise and 10 have reduced Blood Pressure

40 people do not do regular exercise and 30 have high Blood Pressure

Before we can talk about the odds ratio we need to look at probabilities and also clarify which relationship we are examining.

Firstly let us look at some probabilities.

What is the probability that someone who is in the exercise intervention group will have reduced Blood Pressure?

This would be 40/60 or 0.67 (2 significant figures). Just to explain – if someone is in the exercise group then we know that 40 have reduced Blood Pressure and 20 have high Blood Pressure. The probability is the ratio of the outcome of interest to all of the outcomes in that group. Therefore this is 40/60.

What is the probability that someone who is in the exercise intervention group will have high Blood Pressure?

The reasoning is much the same as the example above except we are substituting 20 for 40 i.e. the probability is 20/60 or 0.33 (2 significant figures).

What is the probability that someone who is in the non-exercise group will have lower Blood Pressure?

This will be 10/40 or 0.25

What is the probability that someone who is in the non-exercise group will have high Blood Pressure?

This will be 30/40 or 0.75

Now we can turn to the odds ratio which is the ratio of probabilities.

What is the odds of having high Blood Pressure with exercise compared to non-exercise.

The probability of high Blood Pressure given exercise is 0.33.

The probability of high Blood Pressure given non-exercise is 0.75

The odds ratio of having high Blood Pressure with exercise compared to non-exercise is 0.33/0.75 = 0.44

We can have several odds ratios in the same sample – it depends on what question we are asking.

What is the odds of having lower Blood Pressure with exercise compared to non-exercise.

The probability of lower Blood Pressure given exercise is 0.67

The probability of lower Blood Pressure given exercise is 0.25

The odds ratio of having lower Blood Pressure with exercise compared to non-exercise is 0.67/0.25 = 2.68.

So just to summarise the odds ratio is a ratio of probabilities. You need to work out the probabilities first. Then you need to clearly state the relationship you are interested in and then calculate the ratio of the probabilities for that relationship.

Finally just a few key points.

The odds ratio can be between 0 and infinity. So for example if all the people in the non-exercise intervention group had high Blood Pressure then the odds ratio of having lower Blood Pressure with exercise compared to non-exercise would be infinity (assuming all other figures remained the same).
The odds ratio can be affected by sample bias. So if the sample is not characteristic of the general population and is small then the odds ratio could be abnormally high or low. The confidence interval is usually calculated for the odds ratio although this can be a little complicated.

Other Links

There is a good explanation of the odds ratio in this paper.

Context

Patient Records

Patient records are central to the delivery of healthcare and serve a number of functions including the recording of clinical assessments and interventions. Aggregated data is also utilised at a local and national level to inform commissioning.

Electronic Patient Records

The digitisation of patient records offers a number of advantages over paper based records. These advantages include automated backup of records, reduced use of physical storage space (since paper based notes are switched to servers), off-site access to records using mobile devices and the potential to develop analytical clinical support tools which use computers to process clinical data to help improve clinical decisions. Not all healthcare services have electronic patient records but most providers are moving in this direction.

Getting Electronic Patient Records to Talk to Each Other

When patients move between healthcare providers – for instance between primary care and the hospital – they may find that one provider does not have information that the other provider has. There are many providers and many electronic paper record systems. For two systems to talk to each other they have to solve a number of problems. When these problems are solved a patient can move between providers and healthcare information can be accessed by the different providers. A key solution to this problem of health information gaps is the Health Information Exchange (HIE).

The Health Information Exchange

There are many definitions of what a Health Information Exchange is. (Hersh et al, 2015) define a HIE as follows:

Whilst this definition is simple, the process of sharing clinical information between healthcare organisations is technically complex and encompasses a range of software, hardware and governance issues. The process of helping systems to talk to each other is helped by the development of standards. A set of standards is outlined in the NHS interoperability framework.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

The NMDA Receptor is an ion channel which is activated by Glutamate. The NMDA Receptor is involved in the response of neurons to ischaemia. The NMDA Receptor is also involved in memory formation in a process referred to as Long Term Potentiation.

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

Lai, Zhang and Wang outline the role of Monosodium Glutamate in their paper. Monosodium Glutamate is a food additive. In a paper published in 1957, Lucas and Newhhouse reported the results of their study looking at the effects of Monosodium Glutamate (MSG) when applied to the mouse retina. The researchers found evidence of neurotoxicity. Further findings confirmed that Glutamate (MSG dissociates into Sodium and Glutamate in solution) is excitatory (i.e. increases the chance of a neuron firing).

What is Excitotoxicity?

Excitoxicity is the damage and death of neurons secondary to Glutamate receptor activation. There is an interesting paper by Lai, Zhang and Wang on excitotoxicity and stroke. The authors look at the targets for neuroprotection following a stroke. Excitotoxicity is related to the NMDA Receptor. This in turn is relevant to the Brain Hypometabolism Hypothesis.

In their paper Lai, Zhang and Wang write that although excitotoxicity was initially investigated in relation to the properties of Monosodium Glutamate it plays an important role in brain trauma and a number of neurodegenerative conditions including

Huntington’s Disease

Alzheimer’s Disease

Amyotrophic Lateral Sclerosis

Excitotoxicity and Excitation

Professor John Olney and colleagues conducted research in 1971 into the excitotoxic effects of Glutamate analogues (Olney et al, 1971). They found that analogues which were excitatory were excitotoxic and those which were not excitatory were not excitotoxic. Contextualising this – the effects of Glutamate are mediated via the NMDA Receptor and excitotoxicity is a pathological process which can result from reduced energy metabolism. This in turn is relevant to the Brain Hypometabolism Hypothesis.

Summarising this:

Excitatory properties are required for excitoxicity

Brain Hypometabolism Hypothesis

The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that

‘Energy hypometabolism in the brain leads to neuropathology‘

Key Pathways in Energy Metabolism

There are several key pathways in energy metabolism in humans. Several pathways result in the formation of Acetyl CoA from fatty acids, amino acids and glucose. Acetyl CoA is utilised in the Citric Acid Cycle. The Citric Acid Cycle generates ATP. The Citric Acid Cycle also generates NADH which is used in Oxidative Phosphorylation which utilises Oxygen as an electron acceptor.

What is Glycolysis?

Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.

The Citric Acid Cycle is one of the main energy metabolism pathways in humans. Acetyl Co-A which is generated from other pathways is utilised in the Citric Acid Cycle. The Citric Acid Cycle has a number of properties

Generation of energy in the form of ATP

Generating NADH which is utilised in oxidative phosphorylation

Citric Acid is regenerated

Carbon Dioxide is produced

The Citric Acid Cycle takes place in the Mitochondria.

What is Oxidative Phosphorylation?

Oxidative phosphorylation is a series of chemical reactions in which electrons are transferred, nutrients are metabolised and ATP is formed. Nutrients are oxidised and the donated electrons are processed in the electron transport chain. ATP formation via ATP Synthase utilises the electron/proton gradient across the mitochondrial membrane according to the Chemiosmotic Theory.

What is the Chemiosmotic Theory?

The Chemiosmotic Theory is central to the understanding of Oxidative Phosphorylation. Proposed by Dr Peter Mitchell in 1961, the theory states that the energy for ATP generation derives from electrical and chemical gradients resulting from the transfer of electrons and protons across the mitochondrial membrane in the electron transport chain.

The first step in Oxidative Phosphorylation in humans is the transfer of electrons from NAD via Complex I. The structure of Complex I is shown above. Complex I is also known as NADH-coenzyme Q Oxidoreductase. NADH donates electrons to Complex I in a reaction requiring Coenzyme Q10. The electrons are further transferred via Flavin Mononucleotide and Iron-Sulfur Complexes before the transfer of proteins into the intermembrane space.

Complex II is involved in Oxidative Phosphorylation and is also known as Succinate Dehydrogenase. Succinate is oxidised (donating electrons) to form Fumarate. The donated electrons enter the electron transport chain.

Complex III is also known as Q-cytochrome C Oxidoreductase. Complex III contains Cytochromes. Ubiquinol (a reduced form of Coenzyme Q10) donates electrons to Cytochrome C. Electrons are transferred between molecules in a circuit which causes four protons to be transferred across the Mitochondrial membrane for every 2 electrons. This forms part of the electron transport chain.

ATP Synthase is an enzyme that combines inorganic phosphate and Adenosine Diphosphate to form Adenosine Triphosphate (ATP). This in turn is used as a source of energy.

Complex IV is also known as Cytochrome C Oxidase. Complex IV contains Heme groups, Copper, Magnesium and Zinc. Complex IV facilitates the transfer of electrons to Oxygen in a reaction which results in the formation of water.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

There is an interesting paper on the state of Electronic Health Records and Electronic Information Sharing in the United States published in January 2016 by Jawoom and colleagues.

In a previous post we looked at the calculation of an odds ratio as part of a secondary analysis of the data.

The Odds Ratio calculated was 1.604. This was a comparison of the probability of sharing information with an external provider given access to a certified Electronic Health Record compared to a non-certified Electronic Health Record.

So what does this mean?

A simplistic interpretation is that it is much more likely that if a physician has access to a certified Electronic Health Record (EHR) then they would be more likely to be sharing information electronically with external providers.

Certified EHR’s can have a very specific meaning as this can refer to the Office of the National Coordinator for Health Information Technology criteria for meaningful use. There are two assumptions that are made in linking an affirmative answer to the certified EHR question in the survey to the system being a certified EHR. The first assumption is that the question is interpreted to refer to these criteria and the second is the degree of correlation with an assessment of the EHR for meaningful use. As this was not investigated in the survey, further studies would be needed to understand these correlations.

Nevertheless if we assume direct correlations between the answers and the EHR properties then the implication is that the meaningful use criteria are linked to an increased probability of sharing information electronically with external providers.

The information shared includes images, lab results, problem and medication lists. However the means of sharing electronically is not clarified further. This could for example refer to a Health Information Exchange.

What Does the Odds Ratio Mean?

The odds ratios tells us about a relationship between two things. In the clinical setting these two things might be expected to have a causal relationship e.g. Blood Pressure and exercise.

How is it Calculated?

Taking the Blood Pressure example. Let’s suppose that a group of people have their Blood Pressure checked before and after an exercise/non-exercise intervention. Let’s also suppose that people are classed as doing regular exercise (intervention) or not doing regular exercise (non-exercise).

We want to see if there is a relationship between the two and it would be great if we could have a number to sum up that relationship. Let’s also suppose that we think the relationship is ‘Doing regular exercise reduces Blood Pressure’. The exposure is doing regular exercise and the outcome is reduced Blood Pressure.

Let’s suppose there are 100 people in the study (These are illustrative numbers only). 60 people do regular exercise and 50 people have low Blood Pressure. Of the 60 people that do regular exercise 40 people have low Blood Pressure. I will write this out in the following statements

60 people do regular exercise and 40 have reduced Blood Pressure

60 people do regular exercise and 20 have high Blood Pressure

40 people do not do regular exercise and 10 have reduced Blood Pressure

40 people do not do regular exercise and 30 have high Blood Pressure

Before we can talk about the odds ratio we need to look at probabilities and also clarify which relationship we are examining.

Firstly let us look at some probabilities.

What is the probability that someone who is in the exercise intervention group will have reduced Blood Pressure?

This would be 40/60 or 0.67 (2 significant figures). Just to explain – if someone is in the exercise group then we know that 40 have reduced Blood Pressure and 20 have high Blood Pressure. The probability is the ratio of the outcome of interest to all of the outcomes in that group. Therefore this is 40/60.

What is the probability that someone who is in the exercise intervention group will have high Blood Pressure?

The reasoning is much the same as the example above except we are substituting 20 for 40 i.e. the probability is 20/60 or 0.33 (2 significant figures).

What is the probability that someone who is in the non-exercise group will have lower Blood Pressure?

This will be 10/40 or 0.25

What is the probability that someone who is in the non-exercise group will have high Blood Pressure?

This will be 30/40 or 0.75

Now we can turn to the odds ratio which is the ratio of probabilities.

What is the odds of having high Blood Pressure with exercise compared to non-exercise.

The probability of high Blood Pressure given exercise is 0.33.

The probability of high Blood Pressure given non-exercise is 0.75

The odds ratio of having high Blood Pressure with exercise compared to non-exercise is 0.33/0.75 = 0.44

We can have several odds ratios in the same sample – it depends on what question we are asking.

What is the odds of having lower Blood Pressure with exercise compared to non-exercise.

The probability of lower Blood Pressure given exercise is 0.67

The probability of lower Blood Pressure given exercise is 0.25

The odds ratio of having lower Blood Pressure with exercise compared to non-exercise is 0.67/0.25 = 2.68.

So just to summarise the odds ratio is a ratio of probabilities. You need to work out the probabilities first. Then you need to clearly state the relationship you are interested in and then calculate the ratio of the probabilities for that relationship.

Finally just a few key points.

The odds ratio can be between 0 and infinity. So for example if all the people in the non-exercise intervention group had high Blood Pressure then the odds ratio of having lower Blood Pressure with exercise compared to non-exercise would be infinity (assuming all other figures remained the same).
The odds ratio can be affected by sample bias. So if the sample is not characteristic of the general population and is small then the odds ratio could be abnormally high or low. The confidence interval is usually calculated for the odds ratio although this can be a little complicated.

Other Links

There is a good explanation of the odds ratio in this paper.

Context

Patient Records

Patient records are central to the delivery of healthcare and serve a number of functions including the recording of clinical assessments and interventions. Aggregated data is also utilised at a local and national level to inform commissioning.

Electronic Patient Records

The digitisation of patient records offers a number of advantages over paper based records. These advantages include automated backup of records, reduced use of physical storage space (since paper based notes are switched to servers), off-site access to records using mobile devices and the potential to develop analytical clinical support tools which use computers to process clinical data to help improve clinical decisions. Not all healthcare services have electronic patient records but most providers are moving in this direction.

Getting Electronic Patient Records to Talk to Each Other

When patients move between healthcare providers – for instance between primary care and the hospital – they may find that one provider does not have information that the other provider has. There are many providers and many electronic paper record systems. For two systems to talk to each other they have to solve a number of problems. When these problems are solved a patient can move between providers and healthcare information can be accessed by the different providers. A key solution to this problem of health information gaps is the Health Information Exchange (HIE).

The Health Information Exchange

There are many definitions of what a Health Information Exchange is. (Hersh et al, 2015) define a HIE as follows:

Whilst this definition is simple, the process of sharing clinical information between healthcare organisations is technically complex and encompasses a range of software, hardware and governance issues. The process of helping systems to talk to each other is helped by the development of standards. A set of standards is outlined in the NHS interoperability framework.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

]]>https://theamazingworldofpsychiatry.wordpress.com/2017/08/02/reflections-on-the-odds-ratio-for-the-nchs-data/feed/0Dr Justin Marleycomputer-keyboard-1380475577zzmThe Brain Hypometabolism Hypothesis Part 105: Synaptic and Extrasynaptic NMDA Receptor Differences – Not So Clearhttps://theamazingworldofpsychiatry.wordpress.com/2017/08/01/the-brain-hypometabolism-hypothesis-part-105-synaptic-and-extrasynaptic-nmda-receptor-differences-not-so-clear/
https://theamazingworldofpsychiatry.wordpress.com/2017/08/01/the-brain-hypometabolism-hypothesis-part-105-synaptic-and-extrasynaptic-nmda-receptor-differences-not-so-clear/#commentsTue, 01 Aug 2017 04:23:40 +0000http://theamazingworldofpsychiatry.wordpress.com/?p=18165]]>Lai, Zhang and Wang have written about the NMDA receptor and excitotoxicity in their paper.

Lai et al have outlined a broad division between synaptic and extra-synaptic NMDA receptors. They describe

Synaptic NMDA receptors are pro-survival (of neurons)

Extra-Synaptic NMDA receptors are excitotoxic

They also provide evidence that this division is not so straightforward. There are several lines of evidence that suggest that there is overlap in the NMDA receptor functions across locations.

Thus for example they note that synaptic NMDA-receptor induced Glutamate release is associated with primary hippocampal neuronal death secondary to hypoxic ischaemia and cite (Rothman, 1983 and 1984).

The NMDA Receptor is an ion channel which is activated by Glutamate. The NMDA Receptor is involved in the response of neurons to ischaemia. The NMDA Receptor is also involved in memory formation in a process referred to as Long Term Potentiation.

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

Lai, Zhang and Wang outline the role of Monosodium Glutamate in their paper. Monosodium Glutamate is a food additive. In a paper published in 1957, Lucas and Newhhouse reported the results of their study looking at the effects of Monosodium Glutamate (MSG) when applied to the mouse retina. The researchers found evidence of neurotoxicity. Further findings confirmed that Glutamate (MSG dissociates into Sodium and Glutamate in solution) is excitatory (i.e. increases the chance of a neuron firing).

What is Excitotoxicity?

Excitoxicity is the damage and death of neurons secondary to Glutamate receptor activation. There is an interesting paper by Lai, Zhang and Wang on excitotoxicity and stroke. The authors look at the targets for neuroprotection following a stroke. Excitotoxicity is related to the NMDA Receptor. This in turn is relevant to the Brain Hypometabolism Hypothesis.

In their paper Lai, Zhang and Wang write that although excitotoxicity was initially investigated in relation to the properties of Monosodium Glutamate it plays an important role in brain trauma and a number of neurodegenerative conditions including

Huntington’s Disease

Alzheimer’s Disease

Amyotrophic Lateral Sclerosis

Excitotoxicity and Excitation

Professor John Olney and colleagues conducted research in 1971 into the excitotoxic effects of Glutamate analogues (Olney et al, 1971). They found that analogues which were excitatory were excitotoxic and those which were not excitatory were not excitotoxic. Contextualising this – the effects of Glutamate are mediated via the NMDA Receptor and excitotoxicity is a pathological process which can result from reduced energy metabolism. This in turn is relevant to the Brain Hypometabolism Hypothesis.

Summarising this:

Excitatory properties are required for excitoxicity

Brain Hypometabolism Hypothesis

The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that

‘Energy hypometabolism in the brain leads to neuropathology‘

Key Pathways in Energy Metabolism

There are several key pathways in energy metabolism in humans. Several pathways result in the formation of Acetyl CoA from fatty acids, amino acids and glucose. Acetyl CoA is utilised in the Citric Acid Cycle. The Citric Acid Cycle generates ATP. The Citric Acid Cycle also generates NADH which is used in Oxidative Phosphorylation which utilises Oxygen as an electron acceptor.

What is Glycolysis?

Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.

The Citric Acid Cycle is one of the main energy metabolism pathways in humans. Acetyl Co-A which is generated from other pathways is utilised in the Citric Acid Cycle. The Citric Acid Cycle has a number of properties

Generation of energy in the form of ATP

Generating NADH which is utilised in oxidative phosphorylation

Citric Acid is regenerated

Carbon Dioxide is produced

The Citric Acid Cycle takes place in the Mitochondria.

What is Oxidative Phosphorylation?

Oxidative phosphorylation is a series of chemical reactions in which electrons are transferred, nutrients are metabolised and ATP is formed. Nutrients are oxidised and the donated electrons are processed in the electron transport chain. ATP formation via ATP Synthase utilises the electron/proton gradient across the mitochondrial membrane according to the Chemiosmotic Theory.

What is the Chemiosmotic Theory?

The Chemiosmotic Theory is central to the understanding of Oxidative Phosphorylation. Proposed by Dr Peter Mitchell in 1961, the theory states that the energy for ATP generation derives from electrical and chemical gradients resulting from the transfer of electrons and protons across the mitochondrial membrane in the electron transport chain.

The first step in Oxidative Phosphorylation in humans is the transfer of electrons from NAD via Complex I. The structure of Complex I is shown above. Complex I is also known as NADH-coenzyme Q Oxidoreductase. NADH donates electrons to Complex I in a reaction requiring Coenzyme Q10. The electrons are further transferred via Flavin Mononucleotide and Iron-Sulfur Complexes before the transfer of proteins into the intermembrane space.

Complex II is involved in Oxidative Phosphorylation and is also known as Succinate Dehydrogenase. Succinate is oxidised (donating electrons) to form Fumarate. The donated electrons enter the electron transport chain.

Complex III is also known as Q-cytochrome C Oxidoreductase. Complex III contains Cytochromes. Ubiquinol (a reduced form of Coenzyme Q10) donates electrons to Cytochrome C. Electrons are transferred between molecules in a circuit which causes four protons to be transferred across the Mitochondrial membrane for every 2 electrons. This forms part of the electron transport chain.

ATP Synthase is an enzyme that combines inorganic phosphate and Adenosine Diphosphate to form Adenosine Triphosphate (ATP). This in turn is used as a source of energy.

Complex IV is also known as Cytochrome C Oxidase. Complex IV contains Heme groups, Copper, Magnesium and Zinc. Complex IV facilitates the transfer of electrons to Oxygen in a reaction which results in the formation of water.

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Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

There is an interesting paper on the state of Electronic Health Records and Electronic Information Sharing in the United States published in January 2016 by Jawoom and colleagues.

The data is based on the results of a survey of 10,302 physicians.

As the data is provided this is open data. This enables a secondary analysis.

One key question that can be asked is what is the odds ratio for sharing information with external providers (any ambulatory providers or hospitals) if there is a certified EHR compared to a non-certified EHR in 2014?

Physicians in all-specialities had access to a certified EHR in 74.1% of cases.

Firstly 47.8% of physicians with a certified EHR shared information with external providers. Converting this into a probability – the probability of a physician with a certified EHR sharing with external providers would be 0.478.

Secondly 29.8% of physicians without a certified EHR shared information with external providers. Converting this into a probability – the probability of a physician without a certified EHR sharing with external providers would be 0.298.

We can then ask the question what is the Odds Ratio for sharing information with an external provider given a physician having access to a certified EHR compared to a physician not having access to a certified EHR?

Odds Ratio = 0.478/0.298 = 1.604

What Does the Odds Ratio Mean?

The odds ratios tells us about a relationship between two things. In the clinical setting these two things might be expected to have a causal relationship e.g. Blood Pressure and exercise.

How is it Calculated?

Taking the Blood Pressure example. Let’s suppose that a group of people have their Blood Pressure checked before and after an exercise/non-exercise intervention. Let’s also suppose that people are classed as doing regular exercise (intervention) or not doing regular exercise (non-exercise).

We want to see if there is a relationship between the two and it would be great if we could have a number to sum up that relationship. Let’s also suppose that we think the relationship is ‘Doing regular exercise reduces Blood Pressure’. The exposure is doing regular exercise and the outcome is reduced Blood Pressure.

Let’s suppose there are 100 people in the study (These are illustrative numbers only). 60 people do regular exercise and 50 people have low Blood Pressure. Of the 60 people that do regular exercise 40 people have low Blood Pressure. I will write this out in the following statements

60 people do regular exercise and 40 have reduced Blood Pressure

60 people do regular exercise and 20 have high Blood Pressure

40 people do not do regular exercise and 10 have reduced Blood Pressure

40 people do not do regular exercise and 30 have high Blood Pressure

Before we can talk about the odds ratio we need to look at probabilities and also clarify which relationship we are examining.

Firstly let us look at some probabilities.

What is the probability that someone who is in the exercise intervention group will have reduced Blood Pressure?

This would be 40/60 or 0.67 (2 significant figures). Just to explain – if someone is in the exercise group then we know that 40 have reduced Blood Pressure and 20 have high Blood Pressure. The probability is the ratio of the outcome of interest to all of the outcomes in that group. Therefore this is 40/60.

What is the probability that someone who is in the exercise intervention group will have high Blood Pressure?

The reasoning is much the same as the example above except we are substituting 20 for 40 i.e. the probability is 20/60 or 0.33 (2 significant figures).

What is the probability that someone who is in the non-exercise group will have lower Blood Pressure?

This will be 10/40 or 0.25

What is the probability that someone who is in the non-exercise group will have high Blood Pressure?

This will be 30/40 or 0.75

Now we can turn to the odds ratio which is the ratio of probabilities.

What is the odds of having high Blood Pressure with exercise compared to non-exercise.

The probability of high Blood Pressure given exercise is 0.33.

The probability of high Blood Pressure given non-exercise is 0.75

The odds ratio of having high Blood Pressure with exercise compared to non-exercise is 0.33/0.75 = 0.44

We can have several odds ratios in the same sample – it depends on what question we are asking.

What is the odds of having lower Blood Pressure with exercise compared to non-exercise.

The probability of lower Blood Pressure given exercise is 0.67

The probability of lower Blood Pressure given exercise is 0.25

The odds ratio of having lower Blood Pressure with exercise compared to non-exercise is 0.67/0.25 = 2.68.

So just to summarise the odds ratio is a ratio of probabilities. You need to work out the probabilities first. Then you need to clearly state the relationship you are interested in and then calculate the ratio of the probabilities for that relationship.

Finally just a few key points.

The odds ratio can be between 0 and infinity. So for example if all the people in the non-exercise intervention group had high Blood Pressure then the odds ratio of having lower Blood Pressure with exercise compared to non-exercise would be infinity (assuming all other figures remained the same).
The odds ratio can be affected by sample bias. So if the sample is not characteristic of the general population and is small then the odds ratio could be abnormally high or low. The confidence interval is usually calculated for the odds ratio although this can be a little complicated.

Other Links

There is a good explanation of the odds ratio in this paper.

Context

Patient Records

Patient records are central to the delivery of healthcare and serve a number of functions including the recording of clinical assessments and interventions. Aggregated data is also utilised at a local and national level to inform commissioning.

Electronic Patient Records

The digitisation of patient records offers a number of advantages over paper based records. These advantages include automated backup of records, reduced use of physical storage space (since paper based notes are switched to servers), off-site access to records using mobile devices and the potential to develop analytical clinical support tools which use computers to process clinical data to help improve clinical decisions. Not all healthcare services have electronic patient records but most providers are moving in this direction.

Getting Electronic Patient Records to Talk to Each Other

When patients move between healthcare providers – for instance between primary care and the hospital – they may find that one provider does not have information that the other provider has. There are many providers and many electronic paper record systems. For two systems to talk to each other they have to solve a number of problems. When these problems are solved a patient can move between providers and healthcare information can be accessed by the different providers. A key solution to this problem of health information gaps is the Health Information Exchange (HIE).

The Health Information Exchange

There are many definitions of what a Health Information Exchange is. (Hersh et al, 2015) define a HIE as follows:

Whilst this definition is simple, the process of sharing clinical information between healthcare organisations is technically complex and encompasses a range of software, hardware and governance issues. The process of helping systems to talk to each other is helped by the development of standards. A set of standards is outlined in the NHS interoperability framework.

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Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

The authors distinguish between synaptic and extra-synaptic NMDA receptors. The authors note that a global activation of NMDA receptors can lead to excitoxicity and that this can be inhibited by inhibiting the activation of NMDA receptors containing the N2B subunit (which occur extrasynaptically) (Hardingham et al, 2002).

The NMDA Receptor is an ion channel which is activated by Glutamate. The NMDA Receptor is involved in the response of neurons to ischaemia. The NMDA Receptor is also involved in memory formation in a process referred to as Long Term Potentiation.

In the Brain Hypometabolism Hypothesis there is a focus on the relationship between energy metabolism and neuropathology. The NMDA Receptor and associated metabolic pathways offer a tangible connection between energy metabolism and neuropathology.

Lai, Zhang and Wang outline the role of Monosodium Glutamate in their paper. Monosodium Glutamate is a food additive. In a paper published in 1957, Lucas and Newhhouse reported the results of their study looking at the effects of Monosodium Glutamate (MSG) when applied to the mouse retina. The researchers found evidence of neurotoxicity. Further findings confirmed that Glutamate (MSG dissociates into Sodium and Glutamate in solution) is excitatory (i.e. increases the chance of a neuron firing).

What is Excitotoxicity?

Excitoxicity is the damage and death of neurons secondary to Glutamate receptor activation. There is an interesting paper by Lai, Zhang and Wang on excitotoxicity and stroke. The authors look at the targets for neuroprotection following a stroke. Excitotoxicity is related to the NMDA Receptor. This in turn is relevant to the Brain Hypometabolism Hypothesis.

In their paper Lai, Zhang and Wang write that although excitotoxicity was initially investigated in relation to the properties of Monosodium Glutamate it plays an important role in brain trauma and a number of neurodegenerative conditions including

Huntington’s Disease

Alzheimer’s Disease

Amyotrophic Lateral Sclerosis

Excitotoxicity and Excitation

Professor John Olney and colleagues conducted research in 1971 into the excitotoxic effects of Glutamate analogues (Olney et al, 1971). They found that analogues which were excitatory were excitotoxic and those which were not excitatory were not excitotoxic. Contextualising this – the effects of Glutamate are mediated via the NMDA Receptor and excitotoxicity is a pathological process which can result from reduced energy metabolism. This in turn is relevant to the Brain Hypometabolism Hypothesis.

Summarising this:

Excitatory properties are required for excitoxicity

Brain Hypometabolism Hypothesis

The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that

‘Energy hypometabolism in the brain leads to neuropathology‘

Key Pathways in Energy Metabolism

There are several key pathways in energy metabolism in humans. Several pathways result in the formation of Acetyl CoA from fatty acids, amino acids and glucose. Acetyl CoA is utilised in the Citric Acid Cycle. The Citric Acid Cycle generates ATP. The Citric Acid Cycle also generates NADH which is used in Oxidative Phosphorylation which utilises Oxygen as an electron acceptor.

What is Glycolysis?

Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.

The Citric Acid Cycle is one of the main energy metabolism pathways in humans. Acetyl Co-A which is generated from other pathways is utilised in the Citric Acid Cycle. The Citric Acid Cycle has a number of properties

Generation of energy in the form of ATP

Generating NADH which is utilised in oxidative phosphorylation

Citric Acid is regenerated

Carbon Dioxide is produced

The Citric Acid Cycle takes place in the Mitochondria.

What is Oxidative Phosphorylation?

Oxidative phosphorylation is a series of chemical reactions in which electrons are transferred, nutrients are metabolised and ATP is formed. Nutrients are oxidised and the donated electrons are processed in the electron transport chain. ATP formation via ATP Synthase utilises the electron/proton gradient across the mitochondrial membrane according to the Chemiosmotic Theory.

What is the Chemiosmotic Theory?

The Chemiosmotic Theory is central to the understanding of Oxidative Phosphorylation. Proposed by Dr Peter Mitchell in 1961, the theory states that the energy for ATP generation derives from electrical and chemical gradients resulting from the transfer of electrons and protons across the mitochondrial membrane in the electron transport chain.

The first step in Oxidative Phosphorylation in humans is the transfer of electrons from NAD via Complex I. The structure of Complex I is shown above. Complex I is also known as NADH-coenzyme Q Oxidoreductase. NADH donates electrons to Complex I in a reaction requiring Coenzyme Q10. The electrons are further transferred via Flavin Mononucleotide and Iron-Sulfur Complexes before the transfer of proteins into the intermembrane space.

Complex II is involved in Oxidative Phosphorylation and is also known as Succinate Dehydrogenase. Succinate is oxidised (donating electrons) to form Fumarate. The donated electrons enter the electron transport chain.

Complex III is also known as Q-cytochrome C Oxidoreductase. Complex III contains Cytochromes. Ubiquinol (a reduced form of Coenzyme Q10) donates electrons to Cytochrome C. Electrons are transferred between molecules in a circuit which causes four protons to be transferred across the Mitochondrial membrane for every 2 electrons. This forms part of the electron transport chain.

ATP Synthase is an enzyme that combines inorganic phosphate and Adenosine Diphosphate to form Adenosine Triphosphate (ATP). This in turn is used as a source of energy.

Complex IV is also known as Cytochrome C Oxidase. Complex IV contains Heme groups, Copper, Magnesium and Zinc. Complex IV facilitates the transfer of electrons to Oxygen in a reaction which results in the formation of water.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section

There is an interesting paper on the state of Electronic Health Records and Electronic Information Sharing in the United States published in January 2016 by Jawoom and colleagues.

In their data, the authors ask respondents whether their information is shared electronically with external providers/unaffiliated hospitals.

The figures ranged from 17.7% in New Jersey to 58.8 in North Dakota. The figures from North Dakota suggest that this state may be a leader in the sharing of health information electronically. Although North Dakota wasn’t the state with the highest percentage of respondents reporting that they were using a certified Electronic Health Record, it was close at 81.2%.

This initial data suggests that North Dakota may be an exemplar of electronic sharing of health information sharing and it would be interesting to see the results of further studies in this area.

Context

Patient Records

Patient records are central to the delivery of healthcare and serve a number of functions including the recording of clinical assessments and interventions. Aggregated data is also utilised at a local and national level to inform commissioning.

Electronic Patient Records

The digitisation of patient records offers a number of advantages over paper based records. These advantages include automated backup of records, reduced use of physical storage space (since paper based notes are switched to servers), off-site access to records using mobile devices and the potential to develop analytical clinical support tools which use computers to process clinical data to help improve clinical decisions. Not all healthcare services have electronic patient records but most providers are moving in this direction.

Getting Electronic Patient Records to Talk to Each Other

When patients move between healthcare providers – for instance between primary care and the hospital – they may find that one provider does not have information that the other provider has. There are many providers and many electronic paper record systems. For two systems to talk to each other they have to solve a number of problems. When these problems are solved a patient can move between providers and healthcare information can be accessed by the different providers. A key solution to this problem of health information gaps is the Health Information Exchange (HIE).

The Health Information Exchange

There are many definitions of what a Health Information Exchange is. (Hersh et al, 2015) define a HIE as follows:

Whilst this definition is simple, the process of sharing clinical information between healthcare organisations is technically complex and encompasses a range of software, hardware and governance issues. The process of helping systems to talk to each other is helped by the development of standards. A set of standards is outlined in the NHS interoperability framework.

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section